Respiratory Brucellosis

Madkour, M. Monir; Alsaif, Abdulaziz

doi:10.1007/978-3-642-59533-2_12

Cited by 3 publications

(1 citation statement)

References 46 publications

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“…Pulmonary involvement (as in Case 2) occurs in 1-7% of patients with brucellosis. Bronchitis, interstitial pneumonitis, lobar pneumonia, lung nodules, pleural effusion, hilar lymphadenopathy, empyema, or abscesses have been reported (Pappas et al, 2003;Bosilkovski, 2013), and sometimes it is difficult initially to differentiate respiratory brucellosis from tuberculosis or other community acquired pneumonia forms (Madkour & Al-Saif, 2001;Pappas et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Increased risk of brucellosis misdiagnosis in regions that lose their endemicity

Bosilkovski¹

2023

Trop Biomed

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Over the last decades, the epidemiology of human brucellosis globally has been subjected to significant changes, with the eradication of many existing endemic hot spots. This paper describes three cases with initial misdiagnosis of brucellosis that were managed during 2011-2017 in Republic of North Macedonia, country that until recently has been declared as endemic region. In spite of the fever, constitutional symptoms, focal disease (spondylitis, pneumonia and orchitis) and previous contact with domestic animals, brucellosis was not initially recognized, and patients were inadequately managed. Brucellosis should be part of differential diagnostic considerations in patients exposed to contacts with animals, with osteoarticular symptoms and signs, constitutional manifestations and different organ involvements in endemic regions where its incidence is diminishing.

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Section: Discussionmentioning

confidence: 99%

Increased risk of brucellosis misdiagnosis in regions that lose their endemicity

Bosilkovski¹

2023

Trop Biomed

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Brucella abortus Promotes a Fibrotic Phenotype in Hepatic Stellate Cells, with Concomitant Activation of the Autophagy Pathway

et al. 2018

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The liver is frequently affected in patients with active brucellosis. The present study demonstrates that infection induces the activation of the autophagic pathway in hepatic stellate cells to create a microenvironment that promotes a profibrogenic phenotype through the induction of transforming growth factor-β1 (TGF-β1), collagen deposition, and inhibition of matrix metalloproteinase-9 (MMP-9) secretion. Autophagy was revealed by upregulation of the LC3II/LC3I ratio and Beclin-1 expression as well as inhibition of p62 expression in infected cells. The above-described findings were dependent on the type IV secretion system (VirB) and the secreted BPE005 protein, which were partially corroborated using the pharmacological inhibitors wortmannin, a phosphatidyl inositol 3-kinase inhibitor, and leupeptin plus E64 (inhibitors of lysosomal proteases). Activation of the autophagic pathway in hepatic stellate cells during infection could have an important contribution to attenuating inflammatory hepatic injury by inducing fibrosis. However, with time, infection induced Beclin-1 cleavage with concomitant cleavage of caspase-3, indicating the onset of apoptosis of LX-2 cells, as was confirmed by the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay and Hoechst staining. These results demonstrate that the cross talk of LX-2 cells and induces autophagy and fibrosis with concomitant apoptosis of LX-2 cells, which may explain some potential mechanisms of liver damage observed in human brucellosis.

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Brucella abortus Invasion of Osteocytes Modulates Connexin 43 and Integrin Expression and Induces Osteoclastogenesis via Receptor Activator of NF-κB Ligand and Tumor Necrosis Factor Alpha Secretion

et al. 2016

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Brucella spp. are Gram-negative facultative intracellular bacteria that cause a debilitating and chronic zoonotic disease (1). Osteoarticular complications are important due to their high prevalence and also to the associated functional sequelae (2-4). Bone loss has been consistently reported in the three most frequent forms of osteoarticular brucellosis (sacroiliitis, spondylitis, and peripheral arthritis) (5-8).Although the ability of Brucella to cause bone loss is well documented, the molecular mechanisms implicated have not been completely deciphered yet. We have recently described a putative immune mechanism for inflammatory bone loss that may occur in response to infection by B. abortus. Our results revealed an important contribution of the macrophages, osteoblasts, and T lymphocytes in response to B. abortus infection and the resulting induction of osteoclast differentiation (9-11).For many years the bone-bound osteocyte has been considered a relatively inactive cell with a broadly unknown role in the bone. But osteocytes are not only the most abundant bone cells and comprise up to 95% of the bone cells in the adult skeleton but also the central regulators of the differentiation and activity of both osteoblasts and osteoclasts during bone remodeling (12). Primary osteocytes and the osteocyte cell line MLO-Y4 secrete macrophage colony-stimulating factor (M-CSF) and RANKL, both necessary for osteoclast formation (13), and recent studies showed that osteocytes are the major regulators of osteoclast formation and activation (14). In addition to the role of osteocytes in regulating bone remodeling, emerging evidence suggests an important role for the gap junction in osteoclast-osteocyte communication (15). Connexin 43 (Cx43) is the most prominent gap junction protein expressed in osteocytes (15), and deficient mice have increased bone resorption and osteoclast numbers (16,17). In vitro studies revealed that Cx43-deficient MLO-Y4 cells display an increase in the RANKL/osteoprotegerin (OPG) ratio compared to control MLO-Y4 cell levels, indicating that loss of Cx43 in osteocytes promotes osteoclastogenesis (17,18). On the other hand, it has been reported that mice lacking Cx43 in osteoblasts/osteocytes or only in osteocytes exhibit increased osteocyte apoptosis (18). Moreover, integrins can link the cellular cytoskeletal network to the extracellular matrix (19). Integrins are essential determinants of cell survival, and, in many cases, prevention or alteration of integrin adhesion triggers a form of apoptosis known as anoikis (20). In

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Respiratory Brucellosis

Cited by 3 publications

References 46 publications

Increased risk of brucellosis misdiagnosis in regions that lose their endemicity

Increased risk of brucellosis misdiagnosis in regions that lose their endemicity

Brucella abortus Promotes a Fibrotic Phenotype in Hepatic Stellate Cells, with Concomitant Activation of the Autophagy Pathway

Brucella abortus Invasion of Osteocytes Modulates Connexin 43 and Integrin Expression and Induces Osteoclastogenesis via Receptor Activator of NF-κB Ligand and Tumor Necrosis Factor Alpha Secretion

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